Evaluation of the Iowa Department of Transportation's Compensatory Wetland Mitgation Program, August 30, 2004

The purpose of this investigation was to evaluate the Compensatory Wetland Mitigation Program at the Iowa Department of Transportation (DOT) in terms of regulatory compliance. Specific objectives included: 1) Determining if study sites meet the definition of a jurisdictional wetland. 2) Determining the degree of compliance with requirements specified in Clean Water Act Section 404 permits. A total of 24 study sites, in four age classes were randomly selected from over 80 sites currently managed by the Iowa DOT. Wetland boundaries were delineated in the field and mitigation compliance was determined by comparing the delineated wetland acreage at each study site to the total wetland acreage requirements specified in individual CWA Section 404 permits. Of the 24 sites evaluated in this study, 58 percent meet or exceed Section 404 permit requirements. Net gain ranged from 0.19 acre to 27.2 acres. Net loss ranged from 0.2 acre to 14.6 acres. The Denver Bypass 1 site was the worst performer, with zero acres of wetland present on the site and the Akron Wetland Mitigation Site was the best performer with slightly more than 27 acres over the permit requirement. Five of the 10 under-performing sites are more than five years post construction, two are five years post construction, one is three years post construction and the remaining two are one year post construction. Of the sites that meet or exceed permit requirements, approximately 93 percent are five years or less post construction and approximately 43 percent are only one year old. Only one of the 14 successful sites is more than five years old. Using Section 404 permit acreage requirements as the criteria for measuring success, 58 percent of the wetland mitigation sites investigated as part of this study are successful. Using net gain/loss as the measure of success, the Compensatory Wetland Mitigation Program has been successful in creating/restoring nearly 44 acres of wetland over what was required by permits.

A-Kinase Anchoring Protein Lbc Coordinates a p38 Activating Signaling Complex Controlling Compensatory Cardiac Hypertrophy.

In response to stress, the heart undergoes a remodeling process associated with cardiac hypertrophy that eventually leads to heart failure. A-kinase anchoring proteins (AKAPs) have been shown to coordinate numerous prohypertrophic signaling pathways in cultured cardiomyocytes. However, it remains to be established whether AKAP-based signaling complexes control cardiac hypertrophy and remodeling in vivo. In the current study, we show that AKAP-Lbc assembles a signaling complex composed of the kinases PKN, MLTK, MKK3, and p38α that mediates the activation of p38 in cardiomyocytes in response to stress signals. To address the role of this complex in cardiac remodeling, we generated transgenic mice displaying cardiomyocyte-specific overexpression of a molecular inhibitor of the interaction between AKAP-Lbc and the p38-activating module. Our results indicate that disruption of the AKAP-Lbc/p38 signaling complex inhibits compensatory cardiomyocyte hypertrophy in response to aortic banding-induced pressure overload and promotes early cardiac dysfunction associated with increased myocardial apoptosis, stress gene activation, and ventricular dilation. Attenuation of hypertrophy results from a reduced protein synthesis capacity, as indicated by decreased phosphorylation of 4E-binding protein 1 and ribosomal protein S6. These results indicate that AKAP-Lbc enhances p38-mediated hypertrophic signaling in the heart in response to abrupt increases in the afterload.

Modified Blalock-Taussig shunt with compensatory properties.

Determination of the proper length of the tubular prosthesis is a major issue when performing a systemic-pulmonary artery shunt. The procedure is simplified by using a prosthesis with accordionlike properties. This was demonstrated in 7 consecutive infants with complex congenital heart defects, in whom systemic-pulmonary artery shunts were placed without early or late complications.

Evaluation of the Iowa Department of Transportation's Compensatory Wetland Mitigation Program, TR-500, 2004

The purpose of this investigation was to evaluate the Compensatory Wetland Mitigation Program at the Iowa Department of Transportation (DOT) in terms of regulatory compliance. Specific objectives included: 1) Determining if study sites meet the definition of a jurisdictional wetland. 2) Determining the degree of compliance with requirements specified in Clean Water Act Section 404 permits. A total of 24 study sites, in four age classes were randomly selected from over 80 sites currently managed by the Iowa DOT. Wetland boundaries were delineated in the field and mitigation compliance was determined by comparing the delineated wetland acreage at each study site to the total wetland acreage requirements specified in individual CWA Section 404 permits. Of the 24 sites evaluated in this study, 58 percent meet or exceed Section 404 permit requirements. Net gain ranged from 0.19 acre to 27.2 acres. Net loss ranged from 0.2 acre to 14.6 acres. The Denver Bypass 1 site was the worst performer, with zero acres of wetland present on the site and the Akron Wetland Mitigation Site was the best performer with slightly more than 27 acres over the permit requirement. Five of the 10 under-performing sites are more than five years post construction, two are five years post construction, one is three years post construction and the remaining two are one year post construction. Of the sites that meet or exceed permit requirements, approximately 93 percent are five years or less post construction and approximately 43 percent are only one year old. Only one of the 14 successful sites is more than five years old. Using Section 404 permit acreage requirements as the criteria for measuring success, 58 percent of the wetland mitigation sites investigated as part of this study are successful. Using net gain/loss as the measure of success, the Compensatory Wetland Mitigation Program has been successful in creating/restoring nearly 44 acres of wetland over what was required by permits.

Compensatory up-regulation of angiotensin II subtype 1 receptors in alpha ENaC knockout heterozygous mice.

BACKGROUND: In mice, a partial loss of function of the epithelial sodium channel (ENaC), which regulates sodium excretion in the distal nephron, causes pseudohypoaldosteronism, a salt-wasting syndrome. The purpose of the present experiments was to examine how alpha ENaC knockout heterozygous (+/-) mice, which have only one allele of the gene encoding for the alpha subunit of ENaC, control their blood pressure (BP) and sodium balance. METHODS: BP, urinary electrolyte excretion, plasma renin activity, and urinary adosterone were measured in wild-type (+/+) and heterozygous (+/-) mice on a low, regular, or high sodium diet. In addition, the BP response to angiotensin II (Ang II) and to Ang II receptor blockade, and the number and affinity of Ang II subtype 1 (AT1) receptors in renal tissue were analyzed in both mouse strains on the three diets. RESULTS: In comparison with wild-type mice (+/+), alpha ENaC heterozygous mutant mice (+/-) showed an intact capacity to maintain BP and sodium balance when studied on different sodium diets. However, no change in plasma renin activity was found in response to changes in sodium intake in alpha ENaC +/- mice. On a normal salt diet, heterozygous mice had an increased vascular responsiveness to exogenous Ang II (P < 0.01). Moreover, on a normal and low sodium intake, these mice exhibited an increase in the number of AT1 receptors in renal tissues; their BP lowered markedly during the Ang II receptor blockade (P < 0.01) and there was a clear tendency for an increase in urinary aldosterone excretion. CONCLUSIONS: alpha ENaC heterozygous mice have developed an unusual mechanism of compensation leading to an activation of the renin-angiotensin system, that is, the up-regulation of AT1 receptors. This up-regulation may be due to an increase in aldosterone production.

Contribution of Intronic miR-338-3p and Its Hosting Gene AATK to Compensatory β-Cell Mass Expansion.

The elucidation of the mechanisms directing β-cell mass regeneration and maintenance is of interest, because the deficit of β-cell mass contributes to diabetes onset and progression. We previously found that the level of the microRNA (miRNA) miR-338-3p is decreased in pancreatic islets from rodent models displaying insulin resistance and compensatory β-cell mass expansion, including pregnant rats, diet-induced obese mice, and db/db mice. Transfection of rat islet cells with oligonucleotides that specifically block miR-338-3p activity increased the fraction of proliferating β-cells in vitro and promoted survival under proapoptotic conditions without affecting the capacity of β-cells to release insulin in response to glucose. Here, we evaluated the role of miR-338-3p in vivo by injecting mice with an adeno-associated viral vector permitting specific sequestration of this miRNA in β-cells. We found that the adeno-associated viral construct increased the fraction of proliferating β-cells confirming the data obtained in vitro. miR-338-3p is generated from an intron of the gene coding for apoptosis-associated tyrosine kinase (AATK). Similarly to miR-338-3p, we found that AATK is down-regulated in rat and human islets and INS832/13 β-cells in the presence of the cAMP-raising agents exendin-4, estradiol, and a G-protein-coupled Receptor 30 agonist. Moreover, AATK expression is reduced in islets of insulin resistant animal models and selective silencing of AATK in INS832/13 cells by RNA interference promoted β-cell proliferation. The results point to a coordinated reduction of miR-338-3p and AATK under insulin resistance conditions and provide evidence for a cooperative action of the miRNA and its hosting gene in compensatory β-cell mass expansion.

Combined deletion of cathepsin protease family members reveals compensatory mechanisms in cancer.

Proteases are important for regulating multiple tumorigenic processes, including angiogenesis, tumor growth, and invasion. Elevated protease expression is associated with poor patient prognosis across numerous tumor types. Several multigene protease families have been implicated in cancer, including cysteine cathepsins. However, whether individual family members have unique roles or are functionally redundant remains poorly understood. Here we demonstrate stage-dependent effects of simultaneously deleting cathepsin B (CtsB) and CtsS in a murine pancreatic neuroendocrine tumor model. Early in tumorigenesis, the double knockout results in an additive reduction in angiogenic switching, whereas at late stages, several tumorigenic phenotypes are unexpectedly restored to wild-type levels. We identified CtsZ, which is predominantly supplied by tumor-associated macrophages, as the compensatory protease that regulates the acquired tumor-promoting functions of lesions deficient in both CtsB and CtsS. Thus, deletion of multiple cathepsins can lead to stage-dependent, compensatory mechanisms in the tumor microenvironment, which has potential implications for the clinical consideration of selective versus pan-family cathepsin inhibitors in cancer.

Compensatory embryonic response to allele-specific inactivation of the murine X-linked gene Hcfc1.

Early in female mammalian embryonic development, cells randomly inactivate one of the two X chromosomes to achieve overall equal inactivation of parental X-linked alleles. Hcfc1 is a highly conserved X-linked mouse gene that encodes HCF-1 - a transcriptional co-regulator implicated in cell proliferation in tissue culture cells. By generating a Cre-recombinase inducible Hcfc1 knock-out (Hcfc1(lox)) allele in mice, we have probed the role of HCF-1 in actively proliferating embryonic cells and in cell-cycle re-entry of resting differentiated adult cells using a liver regeneration model. HCF-1 function is required for both extraembryonic and embryonic development. In heterozygous Hcfc1(lox/+) female embryos, however, embryonic epiblast-specific Cre-induced Hcfc1 deletion (creating an Hcfc1(epiKO) allele) around E5.5 is well tolerated; it leads to a mixture of HCF-1-positive and -negative epiblast cells owing to random X-chromosome inactivation of the wild-type or Hcfc1(epiKO) mutant allele. At E6.5 and E7.5, both HCF-1-positive and -negative epiblast cells proliferate, but gradually by E8.5, HCF-1-negative cells disappear owing to cell-cycle exit and apoptosis. Although generating a temporary developmental retardation, the loss of HCF-1-negative cells is tolerated, leading to viable heterozygous offspring with 100% skewed inactivation of the X-linked Hcfc1(epiKO) allele. In resting adult liver cells, the requirement for HCF-1 in cell proliferation was more evident as hepatocytes lacking HCF-1 fail to re-enter the cell cycle and thus to proliferate during liver regeneration. The survival of the heterozygous Hcfc1(epiKO/+) female embryos, even with half the cells genetically compromised, illustrates the developmental plasticity of the post-implantation mouse embryo - in this instance, permitting survival of females heterozygous for an X-linked embryonic lethal allele.

Sex-specific compensatory growth in food-deprived Nile tilapia

Female Nile tilapia incubate fertilized eggs in their mouth until they are released as alevins. Consequently, the female may not eat during this period. Thus, it would be expected that female Nile tilapia are more adapted to recovering from fasting than males, which do not display this behavior. To test this hypothesis we conducted an experiment with two groups of fish consisting of 7 males and 7 females each, with one fish per aquarium. The experiment was divided into three phases involving adjustment of the animals to experimental aquaria (0-15th day), fasting (16th-27th day), and refeeding (27th-42nd day). Compensatory growth performance was assessed by specific growth rate, weight, food conversion efficiency and food intake. Food conversion efficiency increased after fasting with a similar rate for both sexes. However, specific growth rate, food intake and weight gain (%) were significantly higher in males than in females in the refeeding phase. Thus, we conclude that male Nile tilapia can compensate for a fasting period more efficiently than females, refuting our hypothesis. A possible mechanism involved in the greater male compensation is that they presented greater hyperphagia than females, concomitantly with a similar rate of food conversion efficiency for both sexes during refeeding, which would probably be provoking greater growth in males.

Compensatory enlargement of human coronary arteries identified by magnetic resonance imaging

The aim of the present study was to evaluate the role of magnetic resonance imaging (MRI) for the non-invasive detection of coronary abnormalities and specifically the remodeling process in patients with coronary artery disease (CAD). MRI was performed in 10 control healthy subjects and 26 patients with angiographically proven CAD of the right coronary (RCA) or left anterior descending (LAD) artery; 23 patients were within two months of acute coronary syndromes, and 3 had stable angina with a positive test for ischemia. Wall thickness (WT), vessel wall area (VWA), total vessel area (TVA), and luminal area (LA) were measured. There were significant increases in WT (mean ± SEM, RCA: 2.62 ± 0.75 vs 0.53 ± 0.15 mm; LAD: 2.21 ± 0.69 vs 0.62 ± 0.24 mm) and in VWA (RCA: 30.96 ± 17.57 vs 2.1 ± 1.2 mm²; LAD: 19.53 ± 7.25 vs 3.6 ± 2.0 mm²) patients compared to controls (P < 0.001 for each variable). TVA values were also greater in patients compared to controls (RCA: 44.56 ± 21.87 vs 12.3 ± 4.2 mm²; LAD: 31.89 ± 11.31 vs 17.0 ± 6.2 mm²; P < 0.001). In contrast, the LA did not differ between patients and controls for RCA or LAD. When the LA was adjusted for vessel size using the LA/TVA ratio, a significant difference was found: 0.33 ± 0.16 in patients vs 0.82 ± 0.09 in controls (RCA) and 0.38 ± 0.13 vs 0.78 ± 0.06 (LAD) (P < 0.001). As opposed to normal controls, positive remodeling was present in all patients with CAD, as indicated by larger VWA. We conclude that MRI detected vessel wall abnormalities and was an effective tool for the noninvasive evaluation of the atherosclerotic process and coronary vessel wall modifications, including positive remodeling that frequently occurs in patients with acute coronary syndromes.

Compensatory Arm Reactions in Individuals with Parkinson’s Disease

This study examined how perturbation-evoked compensatory arm reactions in individuals with Parkinson’s disease (PD) are influenced by explicit verbal instruction. Ten individuals with PD and 15 older adults without PD responded to surface translations with or without specific instruction to reach for and grasp the handrail. Electromyographic (EMG) and kinematic recordings were taken from the reaching arm. Results showed that individuals with and without PD benefitted similarly from explicit instruction. Explicit instruction resulted in earlier (p=0.005) and larger (p<0.001) medial deltoid EMG responses in comparison to no specific instructions. Compensatory arm reactions also occurred with a higher peak medio-lateral wrist velocity (p<0.001) and higher peak shoulder abduction angular velocity (p<0.001) with explicit instruction. Explicit instruction positively influenced compensatory arm reactions in individuals with and without PD. Future research is needed to determine whether the benefits of instruction persist over time and translate to a loss of balance in real life.

The influence of cognitive resources on compensatory arm responses

The purpose of this study was to determine the influence of an ongoing cognitive task on an individual’s ability to generate a compensatory arm response. Twenty young and 16 older adults recovered their balance from a support surface translation while completing a cognitive (counting) task of varying difficulty. Surface electromyographic (EMG) recordings from the shoulders and kinematics of the right arm were collected to quantify the compensatory arm response. Results indicated that the counting task, regardless of its difficulty as well as the age of the individual, had minimal influence on the onset or magnitude of arm muscle activity that occurred following a loss of balance. In contrast to previous research, this study’s findings suggest that the cortical or cognitive resources utilized by the cognitive task are not relied upon for the generation of compensatory arm responses and that older adults are not disproportionately affected by dual-tasking than young adults.

Compensatory signal processing for profoundly hearing-impaired listeners: the transmission of fundamental frequency

This paper reviews a study to determine the usefulness of signal processing along with lipreading in improving speech perception of profoundly hearing impaired persons.